Prior inhibition of vasoconstrictors normalizes GFR in postobstructed kidneys

Prior inhibition of vasoconstrictors normalizes GFR in postobstructed kidneys. The present studies were designed to analyze the potential contribution of angiotensin II and thromboxane A2 to the remarkable decrease in glomerular filtration rate (GFR) and renal plasma flow observed after unilateral release of 24-hour bilateral ureteral obstruction. Pretreatment of the animals with inhibitors of either thromboxane or angiotensin synthesis for 48 hours prior to and during obstruction eliminated the contribution of these vasoconstrictors. Inhibition of these vasoconstrictors during the period of obstruction results in a greater increase in renal plasma flow and GFR than when inhibition was accomplished after release of the obstruction. These data suggest a greater role for these vasoconstrictors in the decrease in GFR that occurs with obstruction. Simultaneous inhibition of thromboxane and angiotensin production normalized GFR of the postobstructed kidney. Administration of atrial peptide after release of obstruction in the different groups of rats resulted in further increases in GFR, urine flow and absolute sodium excretion. It is suggested that atrial peptide participates in the renal hemodynamic changes that occur in the postobstructed kidney.